Fig. 6From: Human papillomavirus integration transforms chromatin to drive oncogenesisHPV integration dysregulates the epigenome and transcriptome up to 100 kbp away. a Difference in average RPM fold change in cell lines with HPV compared to 10 permuted controls. Each data point assesses the difference at a 10-kbp genomic bin. Color: q-value of t-test comparing the cell line with HPV integration to 10 permutations. Line: generalized additive model [44] regression model on transcription data (RNA-seq; left), chromatin accessibility (ATAC-seq; middle), and CTCF presence (ChIP-seq; right). b Same as (a) but comparing GM12878 Epstein-Barr virus (EBV) integration sites to 2 other lymphoblastoid cell lines. c Complementary cumulative distribution function of number of single nucleotide polymorphisms (SNPs) with allelic imbalance exceeding some threshold within some distance from each HPV integration site. Shown either for the sample with the HPV integration site (red) or the mean in 100 different permutations where we assigned each SNP to a cell type without HPV integration at that genomic position (blue). Error bar indicates ± standard deviation (SD). The 5 facets indicate the distance of SNPs from the HPV integration sites in in base pairsBack to article page